Abstract

According to our audiological data, 90% of tinnitus patients have deficits in inner ear function as a generator of tinnitus, mainly in the outer hair cells (OHC). This can be verified by registration of distortion products of otoacoustic emissions (DPOAE). Thus, the main origin of tinnitus is peripheral, and most patients suffer from accompanying hearing loss, even though it is sometimes mild or subjectively not even felt. Whether or not the tinnitus is disturbing, however, is determined through further auditory processing of the "signal" tinnitus and its psychological validation. With almost 50% of our tinnitus and hyperacusis patients, we find hyperfunctioning of the OHC, possibly originating from reduced or ineffective efferent control in the auditory pathway. Efferent activity can be measured by acoustic stimulation of the contralateral ear, which normally reduces the DPOAE amplitudes via efferent inhibition. DPOAE were recorded with 67 tinnitus patients (127 ears) with and without contralateral acoustic stimulation. Twenty-one persons (41 ears) served as controls. With 64% of the tinnitus patients, DPOAE amplitudes were not reduced significantly, compared with 34% of the controls. The medium amplitude reduction for controls was 1.76 dB, whereas for the tinnitus patients it was significantly less (0.91 dB). For a considerable number of tinnitus patients, efferent control of OHC activity is restricted, but this seems to be confined to a certain type of tinnitus only.

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